期刊
CELL METABOLISM
卷 15, 期 2, 页码 157-170出版社
CELL PRESS
DOI: 10.1016/j.cmet.2011.12.015
关键词
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资金
- National Institutes of Health (NIH) [P20RR018733, R21NS074151]
- National Center for Research Resources
- National Science Foundation (NSF) EPSCoR [EPS-0447479]
- NSF EPSCoR [EPS-0447479]
- National Cancer Institute (NCI) [1R01CA118434-01A2, 3R01 CA118434-02S1]
- University of Louisville CTSPGP
- UCSF/G.W. Hooper Research Foundation
- NCI [R35 CA44338]
- UCSF Hellen Diller Family Comprehensive Cancer Center Pilot Grant
- UCSF Department of Radiology and Biomedical Imaging Seed [10-09]
- Johns Hopkins Brain Science Institute
- Ministerio de Ciencia y Tecnologia [SAF2010-17573]
- Junta de Andalucia, Proyectos de Investigacion de Excelencia, Convocatoria, spain [CVI-6656]
The altered metabolism of tumors has been considered a target for anticancer therapy. However, the relationship between distinct tumor-initiating lesions and anomalies of tumor metabolism in vivo has not been addressed. We report that MYC-induced mouse liver tumors significantly increase both glucose and glutamine catabolism, whereas MET-induced liver tumors use glucose to produce glutamine. Increased glutamine catabolism in MYC-induced liver tumors is associated with decreased levels of glutamine synthetase (Glul) and the switch from Gls2 to Gist glutaminase. In contrast to liver tumors, MYC-induced lung tumors display increased expression of both Glul and Gls1 and accumulate glutamine. We also show that inhibition of Gls1 kills cells that overexpress MYC and catabolize glutamine. Our results suggest that the metabolic profiles of tumors are likely to depend on both the genotype and tissue of origin and have implications regarding the design of therapies targeting tumor metabolism.
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